Ryan S. Gray

Dr. Gray obtained his PhD from University of Texas at Austin in Molecular Cell and Developmental Biology in 2009. Dr. Gray then did postdoctoral training at Johns Hopkins in Baltimore and Washington University School of Medicine in Saint Louis, before returning as faculty in Pediatrics at the UT Austin-Dell Pediatrics Research Institute in 2015. Dr. Gray joined the Nutritional Sciences now as an associate professor in that department. 

Dr. Gray is an associate professor in Nutritional Sciences and Pediatrics at the University of Texas at Austin, Dell Pediatrics Research Institute. His research focuses on the identification of cellular and molecular mechanisms that control the development and homeostasis of the spine and related musculoskeletal tissues. Dr. Gray has been successful in using complementary approaches in both mouse and zebrafish model systems, to reveal processes important for spine disorders such as scoliosis.The goal of my lab is the study of the cellular and molecular mechanisms of spine development and homeostasis using primarily the mouse and zebrafish model systems. We choose to utilize both mouse and zebrafish models to provide complementary approaches to study musculoskeletal development and disease.

We developed conditional mouse models of (i) idiopathic scoliosis (IS) and intervertebral disc herniation by removing Gpr126/Adgrg6 function in osteochondral progenitors (Human Molecular Genetics, 2015 and PLoS Genetics, 2019); and (ii) early-onset scoliosis after conditional ablation of Prmt5 function in the same progenitor cell type (Dis Model Mech. 2019). Together these results promote a model of the essential role of cartilaginous tissues and extracellular matrix or ‘matriosome’ for the pathogenesis of idiopathic scoliosis (Bone Research, 2019).

We are at the forefront of establishing the zebrafish model system to analysis a variety of scoliosis pathologies including congenital malformations (Developmental Biology, 2014) and IS (Development Dynamics, 2014 and Developmental Biology 2020). In an effort to promote gene discovery, we established a forward genetic screen in zebrafish which isolated a novel collection of adult viable scoliosis mutants, which are the focus of ongoing studies. To assist in isolation of the causative mutations in this collection, we help develop robust methods for rapid mapping and variant identification using modern genome sequencing (G3, 2017). Thus far, our studies in zebrafish identified common mechanistic roles for scoliosis and hydrocephalus affecting alterations in the physiology of the cerebrospinal fluid (PLOS Genetics, 2018) and established a novel, essential role for a cerebrospinal canal resident protein component, the ‘Reissner fiber’, which regulates spine morphogenesis downstream of disrupted cerebrospinal fluid flow (Current Biology, 2020). We will continue to use a multi-tiered approach, combining zebrafish, mouse, and cell culture models, informed by human genomic studies, with the goal to inform the diagnosis of pediatric/musculoskeletal diseases and provide avenues for therapeutic interventions of these disorders in humans.